Vasomotor responses of newly developed coronary collateral vessels

1996 ◽  
Vol 271 (2) ◽  
pp. H490-H497 ◽  
Author(s):  
J. W. Kinn ◽  
J. D. Altman ◽  
M. W. Chang ◽  
R. J. Bache
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Coronary Artery ◽  
Retrograde Flow ◽  
Collateral Blood Flow ◽  
Coronary Collateral ◽  
Retrograde Blood Flow ◽  
Vasomotor Activity ◽  
Collateral Vessels ◽  
Oxide Synthase

Well-developed coronary collateral vessels contain an abundant muscular media and can undergo active vasomotion. However, early after coronary occlusion, coronary collateral vessels are thin walled with little smooth muscle, suggesting that vasomotor capability might be limited. Consequently, this study determined whether newly developed coronary collateral vessels have active vasomotor activity and whether endothelial function in these newly developed vessels is impaired. Retrograde blood flow was measured as an index of coronary collateral blood flow approximately 2 wk after embolic occlusion of the anterior descending coronary artery of dogs. Agonists were administered into the left main coronary artery to reach collaterals originating from the left coronary system. Baseline retrograde blood flow was 25.1 +/- 2.7 ml/min and increased to 36.7 +/- 3.7 ml/min after nitroglycerin (6 micrograms.kg-1.min-1, P < 0.05). Cyclooxygenase blockade with indomethacin (5 mg/kg i.v.) decreased retrograde collateral blood flow to 16.8 +/- 2.3 ml/min (P <a 0.05). Subsequent administration of acetylcholine increased retrograde flow to 29.4 +/- 3.7 ml/min (P < 0.05), indicating intact endothelium-mediated vasodilation. Inhibition of nitric oxide synthase with NG-nitro-L-arginine further decreased coronary collateral retrograde flow to 12.0 +/- 2.8 ml/min (P < 0.05) and markedly blunted the response to acetylcholine. These findings demonstrate substantial vasomotor capability even early during coronary collateral development and indicate that both nitric oxide and cyclooxygenase-dependent endothelial mechanisms are intact.

Hyperglycemia reduces coronary collateral blood flow through a nitric oxide-mediated mechanism

2001 ◽  
Vol 281 (5) ◽  
pp. H2097-H2104 ◽  
Author(s):  
Judy R. Kersten ◽  
Wolfgang G. Toller ◽  
John P. Tessmer ◽  
Paul S. Pagel ◽  
David C. Warltier
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Blood Glucose ◽  
Blood Glucose Concentration ◽  
Collateral Blood Flow ◽  
Coronary Collateral ◽  
Retrograde Blood Flow ◽  
Flow Through ◽  
Blood Glucose Concentrations ◽  
Coronary Collateral Blood Flow

We tested the hypothesis that hyperglycemia alters retrograde coronary collateral blood flow by a nitric oxide-mediated mechanism in a canine Ameriod constrictor model of enhanced collateral development. Administration of 15% dextrose to increase blood glucose concentration to 400 or 600 mg/dl decreased retrograde blood flow through the left anterior descending coronary artery to 78 ± 9 and 82 ± 8% of baseline values, respectively. In contrast, saline or l-arginine (400 mg · kg−1 · h−1) had no effect on retrograde flow. Coronary hypoperfusion and 1 h of reperfusion decreased retrograde blood flow similarly in saline- orl-arginine-treated dogs (76 ± 11 and 89 ± 4% of baseline, respectively), but these decreases were more pronounced in hyperglycemic dogs (47 ± 10%). l-Arginine prevented decreases in retrograde coronary collateral blood flow during hyperglycemia (100 ± 5 and 95 ± 6% of baseline at blood glucose concentrations of 400 and 600 mg/dl, respectively) and after coronary hypoperfusion and reperfusion (84 ± 14%). The results suggest that hyperglycemia decreases retrograde coronary collateral blood flow by adversely affecting nitric oxide availability.

Increases in Coronary Collateral Blood Flow Produced by Sevoflurane Are Mediated by Calcium-activated Potassium (BKCa) Channels In Vivo 

2002 ◽  
Vol 97 (3) ◽  
pp. 725-731 ◽  
Author(s):  
Franz Kehl ◽  
John G. Krolikowski ◽  
John P. Tessmer ◽  
Paul S. Pagel ◽  
David C. Warltier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Potassium Channels ◽  
Retrograde Flow ◽  
Nitric Oxide Synthesis ◽  
Collateral Blood Flow ◽  
Bkca Channels ◽  
Coronary Collateral ◽  
Calcium Activated Potassium Channels ◽  
Coronary Collateral Blood Flow

Background Sevoflurane enhances coronary collateral blood flow independent of adenosine triphosphate-regulated potassium channels. The authors tested the hypothesis that this volatile anesthetic increases coronary collateral blood flow by either opening calcium-activated potassium channels or by directly stimulating nitric oxide synthesis in the canine coronary collateral circulation. Methods Twelve weeks after left anterior descending coronary artery ameroid constrictor implantation, barbiturate-anesthetized dogs (n = 22) were instrumented for measurement of hemodynamics and retrograde coronary flow. Dogs received sevoflurane ([0.5 and 1.0 minimum alveolar concentration [MAC]) during intracoronary infusions of drug vehicle (0.9% saline), the calcium-activated potassium channel antagonist iberiotoxin (13 microg/min), or the nitric oxide synthase inhibitor -nitro-l-arginine methyl ester (l-NAME, 300 microg/min). Retrograde coronary collateral blood flow was measured under baseline conditions, during and after administration of sevoflurane, and during intracoronary infusion of bradykinin. Data are mean +/- SEM. Results Sevoflurane increased (* &lt; 0.05) retrograde coronary collateral blood flow (from 65 +/- 11 during control to 67 +/- 12* and 71 +/- 12* ml/min during 0.5 and 1.0 MAC, respectively). Iberiotoxin but not l-NAME attenuated these sevoflurane-induced increases in retrograde flow (6 +/- 1*, 7 +/- 2*, and 3 +/- 2 ml/min during vehicle, l-NAME, and iberiotoxin, respectively). After discontinuation of sevoflurane, retrograde flow returned to baseline values in each group. Bradykinin increased retrograde flow in vehicle- (63 +/- 12 to 69 +/- 12* ml/min) but not in iberiotoxin- (61 +/- 7 to 62 +/- 5 ml/min) or l-NAME-treated dogs (64 +/- 11 to 63 +/- 10 ml/min). Conclusions The results demonstrate that sevoflurane increases coronary collateral blood flow, in part, through activation of calcium-activated potassium channels. This action occurs independent of nitric oxide synthesis.

Response of canine coronary collateral vessels to ergonovine and alpha-adrenergic stimulation

1991 ◽  
Vol 261 (4) ◽  
pp. H1019-H1025 ◽  
Author(s):  
R. J. Bache ◽  
B. Foreman ◽  
P. V. Hautamaa
Keyword(s):  
Coronary Artery ◽  
Adrenergic Blockade ◽  
Collateral Flow ◽  
Retrograde Flow ◽  
Adrenergic Stimulation ◽  
Coronary Collateral ◽  
Adrenergic Activity ◽  
Vessel Growth ◽  
Retrograde Blood Flow ◽  
Collateral Vessels

The ability of moderately well-developed coronary collateral vessels to undergo vasoconstriction in response to alpha-adrenergic stimulation and to ergonovine was studied. Studies were performed in 15 dogs 4-16 wk after embolic occlusion of the left anterior descending coronary artery had been performed to stimulate collateral vessel growth. Interarterial collateral flow was measured as retrograde flow from the cannulated left anterior descending coronary artery, while microvascular collateral flow was measured as continuing tissue flow determined with radioactive microspheres administered during the retrograde flow collection. Studies were performed after beta-adrenergic blockade with propranolol. Neither cardiac sympathetic nerve stimulation nor alpha 1-adrenergic stimulation with phenylephrine caused significant change in retrograde blood flow or myocardial tissue flow. The selective alpha 2-adrenergic agonist, B-HT 933, decreased tissue flow in the collateral-dependent region but did not significantly alter retrograde flow. Although these data indicate that intramural microvascular collateral communications are capable of vasoconstriction in response to alpha 2-adrenergic stimulation, the larger interarterial collaterals are unresponsive to alpha-adrenergic influences. However, under the conditions of the experiment, adrenergic activity did not appear to influence collateral function, since neither alpha 1-adrenergic blockade with prazosin nor alpha 2-adrenergic blockade with rauwolscine altered collateral flow. Ergonovine, 0.2-0.8 microgram.kg-1.min-1, caused a 22 +/- 4% decrease in retrograde flow (P less than 0.01) but did not alter microvascular collateral flow. Thus, of the agents tested, only ergonovine caused vasoconstriction of the large interarterial coronary collateral vessels.

scholarly journals Exercise training enhances multiple mechanisms of relaxation in coronary arteries from ischemic hearts

2013 ◽  
Vol 305 (9) ◽  
pp. H1321-H1331 ◽  
Author(s):  
Rachel R. Deer ◽  
Cristine L. Heaps
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Coronary Artery ◽  
Nitric Oxide Synthase ◽  
Exercise Training ◽  
Coronary Arteries ◽  
Vascular Function ◽  
Channel Inhibition ◽  
Oxide Synthase ◽  
Endothelium Dependent Relaxation

Exercise training of coronary artery disease patients is of considerable interest, since it has been shown to improve vascular function and, thereby, enhance blood flow into compromised myocardial regions. However, the mechanisms underlying exercise-induced improvements in vascular function have not been fully elucidated. We tested the hypothesis that exercise training increases the contribution of multiple mediators to endothelium-dependent relaxation of coronary arteries in the underlying setting of chronic coronary artery occlusion. To induce gradual occlusion, an ameroid constrictor was placed around the proximal left circumflex coronary artery in Yucatan miniature swine. At 8 wk postoperatively, pigs were randomly assigned to sedentary or exercise (treadmill, 5 days/wk) regimens for 14 wk. Exercise training significantly enhanced the contribution of nitric oxide, prostanoids, and large-conductance Ca2+-dependent K+ (BKCa) channels to endothelium-dependent, bradykinin-mediated relaxation in nonoccluded and collateral-dependent arteries. Combined nitric oxide synthase, prostanoid, and BKCa channel inhibition ablated the enhanced relaxation associated with exercise training. Exercise training significantly increased nitric oxide levels in response to bradykinin in endothelial cells isolated from nonoccluded and collateral-dependent arteries. Bradykinin treatment significantly increased PGI2 levels in all artery treatment groups and tended to be further enhanced after nitric oxide synthase inhibition in exercise-trained pigs. No differences were found in whole cell BKCa channel currents, BKCa channel protein levels, or arterial cyclic nucleotide levels. Although redundant, upregulation of parallel vasodilator pathways appears to contribute to enhanced endothelium-dependent relaxation, potentially providing a more refined control of blood flow after exercise training.

Reactive oxygen species are critical mediators of coronary collateral development in a canine model

2003 ◽  
Vol 285 (4) ◽  
pp. H1582-H1589 ◽  
Author(s):  
Weidong Gu ◽  
Dorothee Weihrauch ◽  
Katsuya Tanaka ◽  
John P. Tessmer ◽  
Paul S. Pagel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Flow ◽  
Coronary Artery ◽  
Reactive Oxygen ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Oxygen Species ◽  
Collateral Blood Flow ◽  
Collateral Development ◽  
Coronary Collateral

Recent evidence suggests that reactive oxygen species (ROS) promote proliferation and migration of vascular smooth muscle (VSMC) and endothelial cells (EC). We tested the hypothesis that ROS serve as crucial messengers during coronary collateral development. Dogs were subjected to brief (2 min), repetitive coronary artery occlusions (1/h, 8/day, 21 day duration) in the absence (occlusion, n = 8) or presence of N-acetylcysteine (NAC) (occlusion + NAC, n = 8). A sham group ( n = 8) was instrumented identically but received no occlusions. In separate experiments, ROS generation after a single 2-min coronary artery occlusion was assessed with dihydroethidium fluorescence. Coronary collateral blood flow (expressed as a percentage of normal zone flow) was significantly increased (71 ± 7%) in occlusion dogs after 21 days but remained unchanged (13 ± 3%) in sham dogs. Treatment with NAC attenuated increases in collateral blood flow (28 ± 8%). Brief coronary artery occlusion and reperfusion caused ROS production (256 ± 33% of baseline values), which was abolished with NAC (104 ± 12%). Myocardial interstitial fluid produced tube formation and proliferation of VSMC and EC in occlusion but not in NAC-treated or sham dogs. The results indicate that ROS are critical for the development of the coronary collateral circulation.

Inhaled Anesthetics Alter the Determinants of Coronary Collateral Blood Flow in the Dog

1995 ◽  
Vol 83 (4) ◽  
pp. 799-808. ◽  
Author(s):  
Ronnie Mignella ◽  
Charles W. Buffington
Keyword(s):  
Blood Flow ◽  
Collateral Flow ◽  
Retrograde Flow ◽  
Collateral Blood Flow ◽  
Inhaled Anesthetics ◽  
Coronary Collateral ◽  
Anesthetic Agents ◽  
Arteriolar Resistance ◽  
Inhaled Anesthetic ◽  
Coronary Collateral Blood Flow

Background Whether coronary steal is induced by inhaled anesthetic agents remains controversial in part because multiple factors determine collateral blood flow. Methods We used an established model to determine how halothane, isoflurane, and desflurane affect the hemodynamic determinants of coronary collateral blood flow. Twelve dogs were studied 4-5 weeks after ameroid constrictor implantation. Retrograde flow draining from the occluded artery was measured as an index of collateral flow after antegrade embolization. Pressure in the supplying artery at the origin of the collaterals was estimated with a stop-flow technique. These techniques allow calculation of collateral segment resistance and the resistances of the supply artery upstream and downstream from the origin of the collaterals. Results None of the inhaled anesthetics affected collateral segment resistance. Downstream (arteriolar) resistance of the supplying artery was decreased by desflurane (-45%), isoflurane (-35%), and halothane (-15%), lowering pressure at the origin of the collaterals, an effect that was partially offset by a decrease in upstream resistance. Retrograde flow was unaffected by isoflurane and halothane but decreased by about 20% during desflurane administration. Conclusions Inhaled anesthetics have many effects on segmental resistance and pressure in the coronary circulation. These findings help explain conflicting results from previous studies and provide a useful model for investigating the effects of inhaled agents on small coronary arteries.

Vasomotor properties of immature canine coronary collateral circulation

1987 ◽  
Vol 252 (6) ◽  
pp. H1105-H1111
Author(s):  
P. V. Hautamaa ◽  
X. Z. Dai ◽  
D. C. Homans ◽  
J. F. Robb ◽  
R. J. Bache
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Collateral Circulation ◽  
Adrenergic Blockade ◽  
Collateral Flow ◽  
Adrenergic Stimulation ◽  
Coronary Collateral Circulation ◽  
Alpha Adrenoceptor ◽  
Coronary Collateral ◽  
Retrograde Blood Flow

This study examined the ability of the immature coronary collateral circulation to undergo vasodilation in response to nitroglycerin and vasoconstriction in response to alpha-adrenoceptor stimulation. Studies were performed in 12 anesthetized dogs. Collateral flow was estimated from measurements of retrograde flow from the acutely ligated and cannulated anterior descending branch of the left coronary artery. Antegrade flow into the collateral-dependent myocardium was minimized by embolizing the anterior descending artery with 25-microns microspheres. Drugs to be tested were introduced into the left main coronary artery to reach collateral vessels arising from the left circumflex and septal arteries. Intracoronary administration of nitroglycerin (6 micrograms X kg-1 X min-1) resulted in a 33 +/- 7.7% increase in retrograde blood flow (P less than 0.01) and a 23 +/- 3.8% decrease in calculated collateral resistance (P less than 0.01). No significant change occurred in retrograde blood flow or calculated collateral resistance during cardiac sympathetic nerve stimulation after beta-adrenergic blockade with propranolol, selective alpha-adrenergic stimulation with phenylephrine (1 microgram X kg-1 X min-1), or selective alpha 2-stimulation with BHT 933 (2 micrograms X kg-1 X min-1). Thus, the immature coronary collateral circulation was capable of active vasomotion, as demonstrated by vasodilation in response to nitroglycerin, but did not undergo vasoconstriction in response to alpha-adrenoceptor stimulation.

Endothelial function in well-developed canine coronary collateral vessels

1993 ◽  
Vol 264 (2) ◽  
pp. H567-H572 ◽  
Author(s):  
J. Altman ◽  
D. Dulas ◽  
T. Pavek ◽  
D. D. Laxson ◽  
D. C. Homans ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Left Main Coronary Artery ◽  
Arterial System ◽  
Collateral Flow ◽  
Retrograde Flow ◽  
Left Main ◽  
Coronary Collateral Circulation ◽  
Coronary Collateral ◽  
Collateral Vessels ◽  
Coronary Collateral Blood Flow

This study examined responses of coronary collateral blood flow to endothelial-dependent vasodilators. Studies were performed in 13 dogs 4-6 mo after embolic occlusion of the left anterior descending coronary artery (LAD). Collateral flow was determined as the sum of retrograde flow from the cannulated LAD, and continuing tissue flow was measured with microspheres administered during the retrograde flow collection. Agonists were introduced into the left main coronary artery to reach collaterals arising from the left coronary arterial system. The endothelial-dependent vasodilators acetylcholine and bradykinin caused 21 +/- 7 and 25 +/- 8% increases of collateral flow, respectively (each P < 0.05). This was not different from the 28 +/- 8% increase in collateral flow produced by nitroglycerin. To determine whether vasodilator prostaglandins contributed to the increased collateral flow, studies were performed after cyclooxygenase blockade with indomethacin (5 mg/kg iv). Indomethacin caused a 30 +/- 9% decrease of retrograde flow during basal conditions but did not blunt the maximum collateral flow rates produced by acetylcholine, bradykinin, or nitroglycerin. These data demonstrate intact endothelial-dependent vasodilator mechanisms in the well-developed coronary collateral circulation.

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